Protective effects of vitexin on cadmium-induced renal toxicity in rats |
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Authors: | Muhammad Umar Ijaz Moazama Batool Afsheen Batool KA Al-Ghanimd Sara Zafar Asma Ashraf F Al-Misned Z Ahmed Sabahat Shahzadi Abdul Samad Usman Atique N Al-Mulhm S Mahboob |
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Institution: | 1. Department of Zoology, Wildlife and Fisheries, University of Agriculture, Faisalabad, Pakistan;2. Department of Zoology, Govt. College Women University, Sialkot, Pakistan;3. Rawalpindi Medical University and Allied Hospital, Rawalpindi, Pakistan;4. Department of Zoology, College of Science, King Saud University, Saudi Arabia;5. Department of Botany, Government College, University, Faisalabad, Pakistan;6. Department of Zoology, Government College University, Faisalabad, Pakistan;7. Department of Bioscience and Biotechnology, Chungnam National University, South Korea |
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Abstract: | Cadmium (Cd) is an industrial contaminant that poses severe threats to human and animal health. Vitexin (VIT) is a polyphenolic flavonoid of characteristic pharmacological properties. We explored the curative role of vitexin on Cd-induced mitochondrial-dysfunction in rat renal tissues. Twenty-four rats were equally divided into four groups and designated as control, Cd, Cd + vitexin and vitexin treated groups. The results showed that Cd exposure increased urea and creatinine levels while decreased creatinine clearance. Cd reduced the activities of antioxidant enzymes, i.e., catalase (CAT), superoxide dismutase (SOD), glutathione peroxidase (GPx) and glutathione content in the Cd exposed group. Cd exposure significantly (p < 0.05) elevated the reactive oxygen species (ROS) and Thiobarbituric acid reactive substances (TBARS) levels in rat kidney. Cd also caused a significant (p < 0.05) reduction in the mitochondrial TCA-cycle enzymes, including isocitrate dehydrogenase, succinate dehydrogenase, alpha-ketoglutarate dehydrogenase, and malate-dehydrogenase activities. Besides, mitochondrial respiratory chain enzymes, including NADH-dehydrogenase, coenzyme Q-cytochrome reductase, succinic-coenzyme Q, and cytochrome c-oxidase activities were also decreased under Cd exposure. Cd exposure also damaged the mitochondrial membrane potential (MMP). However, VIT treatment potentially reduced the detrimental effects of Cd in the kidney of rats. In conclusion, our study indicated that the VIT could attenuate the Cd-induced renal toxicity in rats. |
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Keywords: | Cadmium Industrial contaminant Mitochondrial dysfunction Vitexin Antioxidant enzymes |
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